Orthostatic (postural) hypotension: causes, symptoms, diagnosis, treatment

Orthostatic (postural) hypotension is a sharp drop in blood pressure (usually more than 20/10 mm Hg) when the patient makes a vertical position. For a few seconds or longer, fainting, loss of consciousness and confusion, dizziness, and visual impairment may occur. In some patients, serial syncopal conditions are revealed. Physical exercise or copious eating can provoke such conditions. Most other manifestations are related to the underlying cause. Orthostatic hypotension is a manifestation of abnormal regulation of blood pressure caused by various causes, rather than a single disease.

Orthostatic hypotension occurs in 20% of elderly people. More often, it can be present in people with concomitant diseases, mainly hypertension, and in patients who have long had a bed rest. Many falls occur due to unrecognized orthostatic hypotension. Appearances of hypotension are aggravated immediately after eating and stimulating the vagus nerve (for example, after urination, defecation).

The syndrome of postural orthostatic tachycardia (SPOT), or the so-called spontaneous postural tachycardia, or a chronic or idiopathic orthostatic reaction, is a syndrome of pronounced propensity for orthostatic reactions at a young age. The incidence is accompanied by the appearance of tachycardia and various other symptoms (such as weakness, dizziness, inability to exercise, unconsciousness), while BP decreases by a very small amount or does not change. The cause of the syndrome is unknown.

[1], [2], [3], [4], [5], [6], [7]

Causes of orthostatic hypotension

Mechanisms to maintain homeostasis can not cope with the restoration of blood pressure in the event of an afferent, central or efferent link disorder of autonomic reflexes. This can occur with the use of certain drugs, in the event that myocardial contractility or vascular resistance is suppressed, with hypovolemia and dyshormonal conditions.

The most common cause in elderly people is a combination of a decrease in the sensitivity of baroreceptors and arterial lability. Reduced sensitivity of baroreceptors leads to a decrease in the severity of reactions from the heart when taking a vertical position. Paradoxically, however, arterial hypertension may be one of the causes of a decrease in the sensitivity of baroreceptors, increasing the tendency to orthostatic hypotension. Also, hypotension occurs after eating. It can be caused by the synthesis of large amounts of insulin with the use of carbohydrate-containing foods, as well as the outflow of blood to the gastrointestinal tract. This condition is aggravated by alcohol intake.

Causes of orthostatic hypotension 

Neurological (including autonomic dysfunction)
 

Central	Multifocal systemic atrophy (formerly Shi-Dreger syndrome). Parkinson's disease. Strokes (various)
Spinal cord	Aboral dorsal. Transverse myelitis. Tumors
Peripheral	Amyloidosis. Diabetic, alcoholic or food neuropathy. Family autonomic dysfunction (Riley-Dai syndrome). Guillain-Barre syndrome. Paraneoplastic syndromes. Severe autonomic failure (formerly called idiopathic orthostatic hypotension). Surgical sympathectomy

Cardiological

Hypovolemia	Adrenal insufficiency. Dehydration. Blood loss
Violation of the vasomotor tone	Prolonged overwork. Hypokalemia
Cardiac output impairment	Aortic stenosis. Constrictive pericarditis. Heart failure. THEM. Tachy- and bradyarrhythmias
Other	Hyperaldosteronism *. Peripheral venous insufficiency. Pheochromocytoma *

Medicinal products

Vasodilators	Calcium channel blockers. Nitrates
Influencing sympathetic regulation	A-Blockers (prazosin). Antihypertensives (clonidine, methyldopa, reserpine, sometimes P-blockers). Antipsychotic (mainly phenothiazines). Monoamine oxidase inhibitors (iMAO). Tricyclic or tetracyclic antidepressants
Other	Alcohol. Barbiturates. Levodopa (in patients with Parkinson's disease is rare). Loop diuretics (eg, furosemide). Quinidine. Vincristine (due to neurotoxicity)

* It can cause arterial hypotension in a horizontal position. Symptoms are more pronounced at the beginning of treatment.

[8], [9], [10], [11]

Pathophysiology of orthostatic hypotension

Normally, gravitational stress due to rapid rising leads to the movement of a certain volume of blood (0.5 to 1 L) into the veins of the lower limbs and trunk. The subsequent transient decrease in venous return reduces cardiac output and, consequently, blood pressure. The first manifestations may be signs of reduced blood supply to the brain. At the same time, not always a decrease in blood pressure leads to hypoperfusion of the brain.

Baroreceptors of the arch of the aorta and carotid zone react to arterial hypotension by activation of vegetative reflexes aimed at restoration of arterial pressure. The sympathetic nervous system increases heart rate and myocardial contractility. Then the tone of the accumulation veins increases. At the same time, the inhibition of parasympathetic reactions leads to an increase in heart rate. If the patient continues to stand, activation of the renin-angiotensin-aldosterone system and the secretion of antidiuretic hormone (ADH) occur, which results in the retention of sodium and water ions, an increase in the volume of circulating blood.

Diagnosis of orthostatic hypotension

Orthostatic hypotension is diagnosed if there is a decrease in the measured blood pressure and the appearance of clinical signs of arterial hypotension on rising and the disappearance of these symptoms when taking a horizontal position. Reasons need to be identified.

Anamnesis

The patient is interviewed to identify known provoking factors (eg, medication, prolonged bed rest, loss of fluid) and symptoms of autonomic failure [such as changes in mydriasis vision and accommodation disorders, urinary incontinence, nausea, poor heat tolerance (excessive sweating) , impotence]. Other neurological symptoms, disorders of the cardiovascular system, impairment of mental functions should also be noted.

Objective inspection. Measurement of blood pressure and heart rate is carried out after 5 minutes after taking the patient to a horizontal position, as well as on the 1 st and 3 rd minutes after getting up. If the patient can not stand, he is examined in the sitting position. Arterial hypotension without compensatory increase in heart rate (<10 per minute) indicates a violation of reflexes, a pronounced increase (> 100 per minute) - about hypovolemia or, if symptoms develop without hypotension, SPOT. Other findings may be signs of impaired nervous system functions, including parkinsonism.

Additional research methods. Routine studies in this case include ECG, determination of glucose concentration and electrolyte composition of blood plasma. At the same time, these and other studies are usually of little informative as compared to specific clinical symptoms.

It is necessary to clarify the state of the autonomic nervous system. With its normal functioning, an increase in heart rate is noted during inspiration. To clarify the condition, cardiac activity in the patient is monitored during slow and deep breathing (about 5 minutes - inhalation, 7 seconds - exhalation) for 1 minute. The largest interval of RR during exhalation is normally 1.15 times longer than the minimum interval during inspiration. The shortening of the interval indicates a vegetative disorder. Similar differences in duration should be present when comparing the rest period and 10-15-second performance of the Valsalva trial. Patients with an abnormal RR interval or other signs of autonomic dysfunction need further examination to exclude diabetes mellitus, Parkinson's disease, possibly multiple sclerosis and severe autonomic nervous system insufficiency. The latter may require a study of the amount of noradrenaline or vasopressin in the blood plasma in patients in horizontal and vertical positions.

The test with an inclined surface (inclined table) is less variable than the measurement of blood pressure in the vertical and horizontal position, and allows to exclude the effect on the venous return of contractions of the muscles of the legs. The patient can be in a vertical position up to 30-45 minutes, during which a blood pressure measurement is performed. The test can be performed if there is a suspicion of a disorder of autonomic regulation. To exclude drug etiology, the amount or, in general, the use of drugs capable of causing orthostatic hypotension should be reduced.

[12], [13], [14], [15], [16]

Prophylaxis and treatment of orthostatic hypotension

Patients who are forced to comply with prolonged bed rest, should sit down in bed daily and, if possible, perform physical exercises. Patients should rise slowly, from sitting or on their side, receive the required amount of fluid, restrict or even stop using alcohol and perform physical exercises whenever possible. Regular physical exercises of medium intensity lead to an increase in peripheral vascular tone and reduce the deposition of blood. Elderly patients should avoid prolonged standing. Sleep with an elevated head can reduce symptoms due to increased sodium retention and a decrease in nocturia.

Arterial hypotension after meals can often be prevented by reducing the total intake of food and its carbohydrate component, minimizing the intake of alcohol and avoiding a sharp rise after eating.

Tight high bandaging of the legs with an elastic bandage can increase venous return, cardiac output and BP after rising. In severe cases, an inflatable suit, similar to the pilots' anti-gravity suits, can be used to create the necessary compression of the legs and abdomen, especially when there is a pronounced resistance to treatment.

An increase in the sodium content, leading to an increase in the volume of circulating blood, can help reduce symptoms. In the absence of heart failure and arterial hypertension, the content of sodium ions can be increased from 5 to 10 g by simply increasing its consumption with food (more food saturation or taking sodium chloride tablets). This appointment increases the risk of developing heart failure, especially in elderly patients and patients with impaired cardiac function; the appearance of edema caused by this method without the development of heart failure is not considered a contraindication to the continuation of treatment.

Fludrocortisone, a mineralocorticoid causing sodium retention, increasing its content in blood plasma and often reducing the phenomenon of arterial hypotension, is effective only in the case of sufficient intake of sodium into the body. The dose of the drug is 0.1 mg at night, with a weekly increase to 1 mg or until the appearance of peripheral edema. This drug is also able to enhance the peripheral vasoconstrictor effect of sympathetic stimulation. There may be arterial hypertension in the prone position, heart failure, hypokalemia. You may need to take potassium.

Non-steroidal anti-inflammatory drugs (NSAIDs), for example indomethacin 25-50 mg / day, can inhibit prostaglandin-induced vasodilation, increasing peripheral vascular resistance. It should be remembered that NSAIDs can cause damage to the gastrointestinal tract and cause vasopressor reactions (there are reports of the equivalence of taking indomethacin and sympathomimetics).

Propranolol and other b-adrenoblockers can enhance the positive effects of sodium and mineralocorticoid therapy. Blockade with propranolol 6-adrenoreceptors leads to uncontrolled α-adrenergic vasoconstriction, which prevents orthostatic vasodilation in some patients.